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For: Munagala R, Aqil F, Gupta RC. Promising molecular targeted therapies in breast cancer. Indian J Pharmacol 2011;43:236-45. [PMID: 21713084 PMCID: PMC3113372 DOI: 10.4103/0253-7613.81497] [Citation(s) in RCA: 59] [Impact Index Per Article: 4.2] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/28/2010] [Accepted: 02/23/2011] [Indexed: 12/27/2022] Open

For:	Munagala R, Aqil F, Gupta RC. Promising molecular targeted therapies in breast cancer. Indian J Pharmacol 2011;43:236-45. [PMID: 21713084 PMCID: PMC3113372 DOI: 10.4103/0253-7613.81497] [Citation(s) in RCA: 59] [Impact Index Per Article: 4.2] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/28/2010] [Accepted: 02/23/2011] [Indexed: 12/27/2022] Open

Number

Cited by Other Article(s)

Ncube SM, Nagarajan A, Lang D, Sinkala M, Burmeister CA, Serala K, Blackburn J, Prince S. c-Myc, AKT, Hsc70, and the T-Box Transcription Factor TBX3 Form an Important Oncogenic Signaling Axis in Breast Cancer. Mol Cancer Res 2025;23:20-32. [PMID: 39264104 DOI: 10.1158/1541-7786.mcr-23-1031] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/11/2023] [Revised: 04/17/2024] [Accepted: 08/07/2024] [Indexed: 09/13/2024]

Shetty SR, Debnath S, Majumdar K, Rajagopalan M, Ramaswamy A, Das A. Virtual screening, molecular dynamics simulations, and in vitro validation of EGFR inhibitors as breast cancer therapeutics. Bioorg Chem 2024;153:107849. [PMID: 39368144 DOI: 10.1016/j.bioorg.2024.107849] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/26/2024] [Revised: 09/25/2024] [Accepted: 09/26/2024] [Indexed: 10/07/2024]

Abstract

A high abundance of Epidermal Growth Factor Receptor (EGFR) in malignant cells makes them a prospective therapeutic target for basal breast tumors. Although EGFR inhibitors are in development as anticancer therapeutics, there exists limitations due to the dose-limiting cytotoxicity that limits their clinical utilization, thereby necessitating the advancement of effective inhibitors. In the present study, we have developed common pharmacophore hypotheses using 30 known EGFR inhibitors. The best pharmacophore hypothesis DHRRR_1 was utilized for virtual screening (VS) of the Phase database containing 4.3 × 106 fully prepared compounds. The top 1000 hits were further subjected to ADME filtration followed by structure-based VS and Molecular Dynamics (MD) simulation investigations. Based on pharmacophore hypothesis matching, XP glide score, interactions between ligands and active site residues, ADME properties, and MD simulations, the five best hits (SN-01 through SN-05) were preferred for in-vitro cytotoxicity studies. All the molecules except SN-02 exhibited cytotoxicity in Triple Negative Breast Cancer (TNBC) cells. These potential EGFR inhibitors effectively downregulated the EGF-induced proliferation, migration, in-vitro tumorigenic capability, and EGFR activation (pEGFR) in the TNBCs. Additionally, in combination with doxorubicin, the identified EGFR inhibitors significantly decreased the EGF-induced proliferation. SN-04, and SN-05 in the presence of a lower concentration of doxorubicin markedly increased the apoptotic markers expression in the TNBCs, an effect which was comparable to a higher concentration of doxorubicin treatment, alone. These observations suggest that both SN-04 and/or SN-05 can improve the efficacy of chemotherapeutic drug, doxorubicin at a lower concentration to avert the higher dose of chemotherapeutic-induced side effects during breast cancer treatment.

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Saghdani N, El Abbouchi A, El Brahmi N, Idir A, Rachedi KO, Berredjem M, Haloui R, Elkhattabi S, Mouse HA, Ben Hadda T, Bousmina M, Zyad A, El Kazzouli S. Design, synthesis, in-vitro, in-silico, DFT and POM studies of a novel family of sulfonamides as potent anti-triple-negative breast cancer agents. Comput Biol Chem 2024;113:108214. [PMID: 39305691 DOI: 10.1016/j.compbiolchem.2024.108214] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/01/2024] [Revised: 09/04/2024] [Accepted: 09/12/2024] [Indexed: 12/15/2024]

Affiliation(s)

Nassima Saghdani Euromed University of Fes, UEMF, Morocco
Abdelmoula El Abbouchi Euromed University of Fes, UEMF, Morocco
Nabil El Brahmi Euromed University of Fes, UEMF, Morocco
Abderrazak Idir Agro-Industrial and Medical Biotechnology Laboratory, Team of Experimental Oncology and Natural Substances, Faculty of Sciences and Technology, Sultan Moulay Slimane University, Beni-Mellal, Morocco; Science and Technology Team, Higher School of Education and Training, Chouaîb Doukkali University, El Jadida, Morocco
Khadija Otmane Rachedi Laboratory of Applied Organic Chemistry, Synthesis of Biomolecules and Molecular Modelling Group, Faculty of Sciences, Department of Chemistry, Badji-Mokhtar - Annaba University, Box 12, Annaba 23000, Algeria
Malika Berredjem Laboratory of Applied Organic Chemistry, Synthesis of Biomolecules and Molecular Modelling Group, Faculty of Sciences, Department of Chemistry, Badji-Mokhtar - Annaba University, Box 12, Annaba 23000, Algeria
Rachid Haloui Laboratory of Engineering, Systems and Applications, National School of Applied Sciences, Sidi Mohamed Ben Abdellah-Fez University, BP Box 72, Fez, Morocco
Souad Elkhattabi Laboratory of Engineering, Systems and Applications, National School of Applied Sciences, Sidi Mohamed Ben Abdellah-Fez University, BP Box 72, Fez, Morocco
Hassan Ait Mouse Agro-Industrial and Medical Biotechnology Laboratory, Team of Experimental Oncology and Natural Substances, Faculty of Sciences and Technology, Sultan Moulay Slimane University, Beni-Mellal, Morocco
Taibi Ben Hadda Euromed University of Fes, UEMF, Morocco
Mostapha Bousmina Euromed University of Fes, UEMF, Morocco
Abdelmajid Zyad Agro-Industrial and Medical Biotechnology Laboratory, Team of Experimental Oncology and Natural Substances, Faculty of Sciences and Technology, Sultan Moulay Slimane University, Beni-Mellal, Morocco
Saïd El Kazzouli Euromed University of Fes, UEMF, Morocco.

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Rassomakhina NV, Ryazanova AY, Likhov AR, Bruskin SA, Maloshenok LG, Zherdeva VV. Tumor Organoids: The Era of Personalized Medicine. BIOCHEMISTRY. BIOKHIMIIA 2024;89:S127-S147. [PMID: 38621748 DOI: 10.1134/s0006297924140086] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 10/03/2023] [Revised: 11/01/2023] [Accepted: 11/09/2023] [Indexed: 04/17/2024]

Hotani A, Kitabatake K, Tsukimoto M. Extracellular Guanosine and Guanine Nucleotides Decrease Viability of Human Breast Cancer SKBR-3 Cells. Biol Pharm Bull 2024;47:14-22. [PMID: 37880111 DOI: 10.1248/bpb.b23-00402] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/27/2023]

Kumar P, Mangla B, Javed S, Ahsan W, Musyuni P, Sivadasan D, Alqahtani SS, Aggarwal G. A review of nanomaterials from synthetic and natural molecules for prospective breast cancer nanotherapy. Front Pharmacol 2023;14:1149554. [PMID: 37274111 PMCID: PMC10237355 DOI: 10.3389/fphar.2023.1149554] [Citation(s) in RCA: 9] [Impact Index Per Article: 4.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/22/2023] [Accepted: 05/10/2023] [Indexed: 06/06/2023] Open

Ismail A, El-Mahdy HA, Abulsoud AI, Sallam AAM, Eldeib MG, Elsakka EG, Zaki MB, Doghish AS. Beneficial and detrimental aspects of miRNAs as chief players in breast cancer: A comprehensive review. Int J Biol Macromol 2022;224:1541-1565. [DOI: 10.1016/j.ijbiomac.2022.10.241] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/18/2022] [Revised: 10/12/2022] [Accepted: 10/24/2022] [Indexed: 11/05/2022]

Tang Q, Wang S, Di Z, Li H, Xu K, Hu X, Di M. Identification and validation of a prognostic risk model based on caveolin family genes for breast cancer. Front Cell Dev Biol 2022;10:822187. [PMID: 36147736 PMCID: PMC9485841 DOI: 10.3389/fcell.2022.822187] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/25/2021] [Accepted: 07/27/2022] [Indexed: 11/13/2022] Open

Abstract Background: Breast cancer (BC) is the most vicious killer of women’s health and is accompanied by increased incidence and mortality rates worldwide. Many studies have demonstrated that caveolins (CAVs) were abnormally expressed in a variety of tumors and implicated in tumorigenesis and cancer progression. However, the role of CAVs in BC remains somewhat contentious.Methods: We comprehensively explored the expression and prognostic value of CAVs (CAV1-3) in BC utilizing public databases (ONCOMINE, TIMER, UALCAN, and TCGA databases). Then we constructed a prognostic model based on the expression profiles. Also, a prognostic nomogram was built to predict the overall survival (OS). We further investigated the relationship between this signature and immune cell infiltration and the mutational landscape in BC. The R package “pRRophetic” was used to predict chemotherapeutic response in BC patients. Finally, we employed loss-of-function approaches to validate the role of CAVs in BC.Results: We found that CAVs were significantly downregulated in various cancer types, especially in BC. Low CAV expression was closely related to the malignant clinicopathological characteristics and worse OS and relapse-free survival (RFS) in BC. Then we constructed a prognostic model based on the expression profiles of CAVs, which divided BC patients into two risk groups. The Kaplan–Meier analysis showed that patients in the high-risk group tend to have a poorer prognosis than those in the low-risk group. Multivariate analysis indicated that the risk score and stage were both independent prognostic factors for BC patients, suggesting a complementary value. The clinical profiles and risk module were used to construct a nomogram that could accurately predict the OS in BC. In addition, we found that patients in the low-risk group tend to have a relatively high immune status and a lower mutation event frequency compared to the high-risk group. Furthermore, this signature could predict the response to chemotherapy and immunotherapy. Finally, CAV depletion promoted the colony formation, migration, and invasion of BC cells.Conclusion: CAVs may serve as novel biomarkers and independent prognostic factors for BC patients. Also, the constructed signature based on CAVs may predict immunotherapeutic responses and provide a novel nomogram for precise outcome prediction of BC. Collapse

Fujihara M, Shien T, Shien K, Suzawa K, Takeda T, Zhu Y, Mamori T, Otani Y, Yoshioka R, Uno M, Suzuki Y, Abe Y, Hatono M, Tsukioki T, Takahashi Y, Kochi M, Iwamoto T, Taira N, Doihara H, Toyooka S. YES1 as a Therapeutic Target for HER2-Positive Breast Cancer after Trastuzumab and Trastuzumab-Emtansine (T-DM1) Resistance Development. Int J Mol Sci 2021;22:ijms222312809. [PMID: 34884609 PMCID: PMC8657782 DOI: 10.3390/ijms222312809] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/08/2021] [Revised: 11/19/2021] [Accepted: 11/24/2021] [Indexed: 01/16/2023] Open

Affiliation(s)

Miwa Fujihara Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan; (M.F.); (K.S.); (K.S.); (Y.Z.); (T.M.); (Y.O.); (R.Y.); (M.U.); (Y.S.); (Y.A.); (M.H.); (T.T.); (Y.T.); (M.K.); (T.I.); (N.T.); (H.D.); (S.T.)
Tadahiko Shien Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan; (M.F.); (K.S.); (K.S.); (Y.Z.); (T.M.); (Y.O.); (R.Y.); (M.U.); (Y.S.); (Y.A.); (M.H.); (T.T.); (Y.T.); (M.K.); (T.I.); (N.T.); (H.D.); (S.T.) Correspondence: ; Tel.: +81-86-235-7265
Kazuhiko Shien Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan; (M.F.); (K.S.); (K.S.); (Y.Z.); (T.M.); (Y.O.); (R.Y.); (M.U.); (Y.S.); (Y.A.); (M.H.); (T.T.); (Y.T.); (M.K.); (T.I.); (N.T.); (H.D.); (S.T.)
Ken Suzawa Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan; (M.F.); (K.S.); (K.S.); (Y.Z.); (T.M.); (Y.O.); (R.Y.); (M.U.); (Y.S.); (Y.A.); (M.H.); (T.T.); (Y.T.); (M.K.); (T.I.); (N.T.); (H.D.); (S.T.)
Tatsuaki Takeda Departments of Pharmacy, Okayama University Hospital, Okayama 700-8558, Japan;
Yidan Zhu Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan; (M.F.); (K.S.); (K.S.); (Y.Z.); (T.M.); (Y.O.); (R.Y.); (M.U.); (Y.S.); (Y.A.); (M.H.); (T.T.); (Y.T.); (M.K.); (T.I.); (N.T.); (H.D.); (S.T.)
Tomoka Mamori Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan; (M.F.); (K.S.); (K.S.); (Y.Z.); (T.M.); (Y.O.); (R.Y.); (M.U.); (Y.S.); (Y.A.); (M.H.); (T.T.); (Y.T.); (M.K.); (T.I.); (N.T.); (H.D.); (S.T.)
Yusuke Otani Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan; (M.F.); (K.S.); (K.S.); (Y.Z.); (T.M.); (Y.O.); (R.Y.); (M.U.); (Y.S.); (Y.A.); (M.H.); (T.T.); (Y.T.); (M.K.); (T.I.); (N.T.); (H.D.); (S.T.)
Ryo Yoshioka Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan; (M.F.); (K.S.); (K.S.); (Y.Z.); (T.M.); (Y.O.); (R.Y.); (M.U.); (Y.S.); (Y.A.); (M.H.); (T.T.); (Y.T.); (M.K.); (T.I.); (N.T.); (H.D.); (S.T.)
Maya Uno Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan; (M.F.); (K.S.); (K.S.); (Y.Z.); (T.M.); (Y.O.); (R.Y.); (M.U.); (Y.S.); (Y.A.); (M.H.); (T.T.); (Y.T.); (M.K.); (T.I.); (N.T.); (H.D.); (S.T.)
Yoko Suzuki Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan; (M.F.); (K.S.); (K.S.); (Y.Z.); (T.M.); (Y.O.); (R.Y.); (M.U.); (Y.S.); (Y.A.); (M.H.); (T.T.); (Y.T.); (M.K.); (T.I.); (N.T.); (H.D.); (S.T.)
Yuko Abe Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan; (M.F.); (K.S.); (K.S.); (Y.Z.); (T.M.); (Y.O.); (R.Y.); (M.U.); (Y.S.); (Y.A.); (M.H.); (T.T.); (Y.T.); (M.K.); (T.I.); (N.T.); (H.D.); (S.T.)
Minami Hatono Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan; (M.F.); (K.S.); (K.S.); (Y.Z.); (T.M.); (Y.O.); (R.Y.); (M.U.); (Y.S.); (Y.A.); (M.H.); (T.T.); (Y.T.); (M.K.); (T.I.); (N.T.); (H.D.); (S.T.)
Takahiro Tsukioki Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan; (M.F.); (K.S.); (K.S.); (Y.Z.); (T.M.); (Y.O.); (R.Y.); (M.U.); (Y.S.); (Y.A.); (M.H.); (T.T.); (Y.T.); (M.K.); (T.I.); (N.T.); (H.D.); (S.T.)
Yuko Takahashi Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan; (M.F.); (K.S.); (K.S.); (Y.Z.); (T.M.); (Y.O.); (R.Y.); (M.U.); (Y.S.); (Y.A.); (M.H.); (T.T.); (Y.T.); (M.K.); (T.I.); (N.T.); (H.D.); (S.T.)
Mariko Kochi Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan; (M.F.); (K.S.); (K.S.); (Y.Z.); (T.M.); (Y.O.); (R.Y.); (M.U.); (Y.S.); (Y.A.); (M.H.); (T.T.); (Y.T.); (M.K.); (T.I.); (N.T.); (H.D.); (S.T.)
Takayuki Iwamoto Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan; (M.F.); (K.S.); (K.S.); (Y.Z.); (T.M.); (Y.O.); (R.Y.); (M.U.); (Y.S.); (Y.A.); (M.H.); (T.T.); (Y.T.); (M.K.); (T.I.); (N.T.); (H.D.); (S.T.)
Naruto Taira Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan; (M.F.); (K.S.); (K.S.); (Y.Z.); (T.M.); (Y.O.); (R.Y.); (M.U.); (Y.S.); (Y.A.); (M.H.); (T.T.); (Y.T.); (M.K.); (T.I.); (N.T.); (H.D.); (S.T.)
Hiroyoshi Doihara Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan; (M.F.); (K.S.); (K.S.); (Y.Z.); (T.M.); (Y.O.); (R.Y.); (M.U.); (Y.S.); (Y.A.); (M.H.); (T.T.); (Y.T.); (M.K.); (T.I.); (N.T.); (H.D.); (S.T.)
Shinichi Toyooka Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan; (M.F.); (K.S.); (K.S.); (Y.Z.); (T.M.); (Y.O.); (R.Y.); (M.U.); (Y.S.); (Y.A.); (M.H.); (T.T.); (Y.T.); (M.K.); (T.I.); (N.T.); (H.D.); (S.T.)

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Immunotherapy for Breast Cancer Treatment. IRANIAN BIOMEDICAL JOURNAL 2021. [PMID: 33724757 PMCID: PMC8183391 DOI: 10.52547/ibj.25.3.140] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Indexed: 02/08/2023]

Yu Q, Li Y, Peng S, Li J, Qin X. Exosomal-mediated transfer of OIP5-AS1 enhanced cell chemoresistance to trastuzumab in breast cancer via up-regulating HMGB3 by sponging miR-381-3p. Open Med (Wars) 2021;16:512-525. [PMID: 33821219 PMCID: PMC8010158 DOI: 10.1515/med-2021-0249] [Citation(s) in RCA: 17] [Impact Index Per Article: 4.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/26/2020] [Revised: 01/28/2021] [Accepted: 02/12/2021] [Indexed: 02/07/2023] Open

Abstract

Background

Long noncoding RNA OPA-interacting protein 5 antisense transcript 1 (OIP5-AS1) was confirmed to involve in the malignancy of breast cancer. However, whether exosomal OIP5-AS1 is implicated in trastuzumab resistance remains unclear.

Methods

The IC₅₀ value of cells to trastuzumab, cell proliferation, migration, and apoptosis was analyzed by cell counting kit-8 assay, colony formation assay, transwell assay, or flow cytometry, respectively. The expression of OIP5-AS1 and microRNA (miR)-381-3p was detected using quantitative real-time polymerase chain reaction. Exosomes were isolated by ultracentrifugation and qualified by nanoparticle tracking analysis software. Western blot was used to detect the protein levels of tumor susceptibility gene 101 (TSG101), CD81, CD63, or high-mobility group protein B3 (HMGB3). The interaction between miR-381-3p and OIP5-AS1 or HMGB3 was confirmed by dual-luciferase reporter assay and pull-down assay. In vivo experiments were conducted using murine xenograft models.

Results

OIP5-AS1 was elevated in trastuzumab-resistant breast cancer cells, and OIP5-AS1 knockdown rescued trastuzumab sensitivity. Extracellular OIP5-AS1 was packaged into exosomes, which were secreted by trastuzumab-resistant cells, and could be absorbed by trastuzumab-sensitive cells in breast cancer. Importantly, intercellular transfer of OIP5-AS1 via exosomes enhanced trastuzumab resistance in vitro. OIP5-AS1 was a sponge of miR-381-3p; besides, miR-381-3p targeted HMGB3. Murine xenograft analysis showed exosomal OIP5-AS1 induced trastuzumab resistance in vivo. Exosomal OIP5-AS1 was dysregulated in the serum of breast cancer patients and might be a promising diagnostic biomarker in trastuzumab resistance.

Conclusion

Intercellular transfer of OIP5-AS1 by exosomes enhanced trastuzumab resistance in breast cancer via miR-381-3p/HMGB3 axis, indicating a potential therapeutic strategy to boost the effectiveness of trastuzumab in resistant breast cancer patients.

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Nagata T, Kanamori M, Sekine S, Arai M, Moriyama M, Fujii T. Clinical study of modulated electro-hyperthermia for advanced metastatic breast cancer. Mol Clin Oncol 2021;14:103. [PMID: 33796292 PMCID: PMC8010507 DOI: 10.3892/mco.2021.2265] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/28/2020] [Accepted: 03/05/2021] [Indexed: 11/06/2022] Open

Simonian M, Haji Ghaffari M, Negahdari B. Immunotherapy for Breast Cancer Treatment. IRANIAN BIOMEDICAL JOURNAL 2021;25:140-156. [PMID: 33724757 PMCID: PMC8183391 DOI: 10.29252/ibj.25.3.140] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Figures] [Subscribe] [Scholar Register] [Received: 07/27/2020] [Accepted: 10/12/2020] [Indexed: 06/12/2023]

Rajaratinam H, Rasudin NS, Al Astani TAD, Mokhtar NF, Yahya MM, Wan Zain WZ, Asma-Abdullah N, Mohd Fuad WE. Breast cancer therapy affects the expression of antineonatal Nav1.5 antibodies in the serum of patients with breast cancer. Oncol Lett 2021;21:108. [PMID: 33376541 PMCID: PMC7751336 DOI: 10.3892/ol.2020.12369] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/11/2020] [Accepted: 11/05/2020] [Indexed: 11/06/2022] Open

Abstract

Neonatal Nav1.5 (nNav1.5) is the alternative splice variant of Nav1.5 and it has been widely associated with the progression of breast cancer. The immunological context of nNav1.5 with respect to breast cancer metastases remains unexplored. The presence of antibodies against nNav1.5 may highlight the immunogenicity of nNav1.5. Hence, the aim of the present study was to detect the presence of antineonatal Nav1.5 antibodies (antinNav1.5-Ab) in the serum of patients with breast cancer and to elucidate the effects of breast cancer therapy on its expression. A total of 32 healthy female volunteers and 64 patients with breast cancer were randomly recruited into the present study as the control and breast cancer group, respectively. Patients with breast cancer were divided equally based on their pre- and ongoing-treatment status. Serum samples were tested with in-house indirect enzyme-linked immunosorbent assay (ELISA) to detect antinNav1.5-Ab, CD25 (T regulatory cell marker) using an ELISA kit and Luminex assay to detect the expression of metastasis-associated cytokines, such as vascular endothelial growth factor (VEGF), interleukin (IL)-6, IL-10, IL-8, chemokine (C-C motif) ligand 2 and tumor necrosis factor-alpha (TNF-α) The mean difference in the expression of antinNav1.5-Ab among the three groups (control, pretreatment and ongoing-treatment) was significant (P=0.0005) and the pretreatment breast cancer group exhibited the highest expression. The concentration of CD25 was highest in the pretreatment breast cancer group compared with the control and ongoing-treatment groups. There was a significant positive correlation between antinNav1.5-Ab and IL-6 in the pretreatment group (r=0.7260; P=0.0210) and a significant negative correlation between antinNav1.5-Ab and VEGF in the ongoing-treatment group (r=-0.842; P-value=0.0040). The high expression of antinNav1.5-Ab in the pretreatment group was in accordance with the uninterrupted presence of metastasis and highlighted the immunogenicity of nNav1.5 whereas the low expression of antinNav1.5-Ab in the ongoing-treatment group reflected the efficacy of breast cancer therapy in eliminating metastases. The augmented manifestation of T regulatory cells in the pretreatment group highlighted the functional role of nNav1.5 in promoting metastasis. The parallel expression of antinNav1.5-Ab with the imbalanced expression of cytokines promoting metastasis (IL-8, IL-6 and TNF-α) and cytokines that prevent metastasis (IL-10) indicated the role of nNav1.5 in breast cancer growth. The expression of antinNav1.5-Ab in accordance to the metastatic microenvironment indicates the immunogenicity of the protein and highlights the influence of breast cancer therapy on its expression level.

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Chong ZX, Yeap SK, Ho WY. Role of miRNAs in regulating responses to radiotherapy in human breast cancer. Int J Radiat Biol 2021;97:289-301. [PMID: 33356761 DOI: 10.1080/09553002.2021.1864048] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/24/2022]

Dual cancer targeting using estrogen functionalized chitosan nanoparticles loaded with doxorubicin-estrone conjugate: A quality by design approach. Int J Biol Macromol 2020;164:2881-2894. [DOI: 10.1016/j.ijbiomac.2020.08.172] [Citation(s) in RCA: 14] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/26/2020] [Revised: 08/14/2020] [Accepted: 08/21/2020] [Indexed: 12/15/2022]

Experimental Models as Refined Translational Tools for Breast Cancer Research. Sci Pharm 2020. [DOI: 10.3390/scipharm88030032] [Citation(s) in RCA: 20] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open

Thiazole-containing compounds as therapeutic targets for cancer therapy. Eur J Med Chem 2019;188:112016. [PMID: 31926469 DOI: 10.1016/j.ejmech.2019.112016] [Citation(s) in RCA: 192] [Impact Index Per Article: 32.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/04/2019] [Revised: 12/20/2019] [Accepted: 12/26/2019] [Indexed: 12/13/2022]

Malliappan SP, Kandasamy P, Chidambaram S, Venkatasubbu D, Perumal SK, Sugumaran A. Breast Cancer Targeted Treatment Strategies: Promising Nanocarrier Approaches. Anticancer Agents Med Chem 2019;20:1300-1310. [PMID: 31642415 DOI: 10.2174/1871520619666191022175003] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/05/2019] [Revised: 08/20/2019] [Accepted: 08/20/2019] [Indexed: 12/18/2022]

Vemuri SK, Banala RR, Mukherjee S, Uppula P, GPV S, A.V. GR, T. M. Novel biosynthesized gold nanoparticles as anti-cancer agents against breast cancer: Synthesis, biological evaluation, molecular modelling studies. MATERIALS SCIENCE & ENGINEERING. C, MATERIALS FOR BIOLOGICAL APPLICATIONS 2019;99:417-429. [DOI: 10.1016/j.msec.2019.01.123] [Citation(s) in RCA: 40] [Impact Index Per Article: 6.7] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Received: 06/14/2018] [Revised: 01/21/2019] [Accepted: 01/27/2019] [Indexed: 01/07/2023]

Sharma D, Bansal KK, Sharma A, Pathak M, Sharma PC. A Brief Literature and Review of Patents on Thiazole Related Derivatives. ACTA ACUST UNITED AC 2019. [DOI: 10.2174/1573407214666180827094725] [Citation(s) in RCA: 16] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/15/2022]

Transcriptional activation of EGFR by HOXB5 and its role in breast cancer cell invasion. Biochem Biophys Res Commun 2018;503:2924-2930. [PMID: 30115380 DOI: 10.1016/j.bbrc.2018.08.071] [Citation(s) in RCA: 23] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/03/2018] [Accepted: 08/07/2018] [Indexed: 12/25/2022]

Mandel A, Larsson P, Sarwar M, Semenas J, Syed Khaja AS, Persson JL. The interplay between AR, EGF receptor and MMP-9 signaling pathways in invasive prostate cancer. Mol Med 2018;24:34. [PMID: 30134822 PMCID: PMC6020326 DOI: 10.1186/s10020-018-0035-4] [Citation(s) in RCA: 30] [Impact Index Per Article: 4.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/23/2018] [Accepted: 06/11/2018] [Indexed: 12/17/2022] Open

Abstract

Background

Metastatic Prostate cancer (PCa) cells have gained survival and invasive advantages. Epidermal growth factor (EGF) receptor is a receptor tyrosine kinase, which may mediate signalling to promote progression and invasion of various cancers. In this study, we uncovered the molecular mechanisms underlying the interconnection among the androgen receptor (AR), matrix metalloproteinase-9 (MMP9) and EGFR in promoting PCa progression.

Methods

Immunohistochemical analysis of the tissue microarrays consisting of primary and metastatic PCa tissues was performed. The clinical importance of EGFR and its association with survivals were analyzed using three cohorts from MSKCC Prostate Oncogenome Project dataset (For primary tumors, n = 181; for metastatic tumors n = 37) and The Cancer Genome Atlas Prostate Adenocarcinoma Provisional dataset (n = 495). Targeted overexpression or inhibition of the proteins of interests was introduced into PCa cell lines. Treatment of PCa cell lines with the compounds was conducted. Immunoblot analysis was performed.

Results

We showed that AR, MMP-9 and EGFR are interconnect factors, which may cooperatively promote PCa progression. Altered EGFR expression was associated with poor disease-free survival in PCa patients. Induced overexpression of AR led to an increase in the expression of EGFR, p-GSK-3β and decrease in p27 expression in PCa cell lines in the presence of androgen stimulation. Overexpression of MMP9 significantly induced EGFR expression in PCa cells. Inhibition of PIP5K1α, a lipid kinase that acts upstream of PI3K/AKT greatly reduced expressions of AR, MMP-9 and EGFR.

Conclusions

Our findings also suggest that PCa cells may utilize AR, EGFR and MMP-9 pathways in androgen-dependent as well as in castration-resistant conditions. Our data suggest a new therapeutic potential to block cancer metastasis by targeting AR, EGFR and MMP-9 pathways in subsets of PCa patients.

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Foo JB, Low ML, Lim JH, Lor YZ, Zainol Abidin R, Eh Dam V, Abdul Rahman N, Beh CY, Chan LC, How CW, Tor YS, Saiful Yazan L. Copper complex derived from S-benzyldithiocarbazate and 3-acetylcoumarin induced apoptosis in breast cancer cell. Biometals 2018;31:505-515. [PMID: 29623473 DOI: 10.1007/s10534-018-0096-4] [Citation(s) in RCA: 22] [Impact Index Per Article: 3.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/29/2017] [Accepted: 03/21/2018] [Indexed: 01/04/2023]

Abstract

Copper complexes have been widely studied for the anti-tumour application as cancer cells are reported to take up greater amounts of copper than normal cells. Preliminary study revealed that the newly synthesised copper complex [Cu(SBCM)₂] displayed marked anti-proliferative towards triple-negative MDA-MB-231 breast cancer cells. Therefore, Cu(SBCM)₂ has great potential to be developed as an agent for the management of breast cancer. The present study was carried out to investigate the mode of cell death induced by Cu(SBCM)₂ towards MDA-MB-231 breast cancer cells. The inhibitory and morphological changes of MDA-MB-231 cells treated with Cu(SBCM)₂ was determined by using MTT assay and inverted light microscope, respectively. The safety profile of Cu(SBCM)₂ was also evaluated towards human dermal fibroblast (HDF) normal cells. Confirmation of apoptosis and cell cycle arrest were determined by flow cytometry analysis. The expression of p53, Bax, Bcl-2 and MMP2 protein were detected with western blot analysis. Cu(SBCM)₂ significantly inhibited the growth of MDA-MB-231 cells in a dose-dependent manner with GI₅₀ 18.7 ± 3.06 µM. Indeed, Cu(SBCM)₂ was less toxic towards HDF normal cells with GI₅₀ 31.8 ± 4.0 µM. Morphological study revealed that Cu(SBCM)₂-treated MDA-MB-231 cells experienced cellular shrinkage, membrane blebbing, chromatin condensation and formation of apoptotic bodies, suggesting that Cu(SBCM)₂ induced apoptosis in the cells, which was confirmed by Annexin-V/PI flow cytometry analysis. It was also found that Cu(SBCM)₂ induced G₂/M phase cell cycle arrest towards MDA-MB-231 cells. The induction of apoptosis and cell cycle arrest in the present study is possibly due to the down-regulation of the mutant p53 and MMP2 protein. In conclusion, Cu(SBCM)₂ can be developed as a targeted therapy for the treatment of triple-negative breast cancer.

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Affiliation(s)

Jhi Biau Foo Faculty of Pharmacy, MAHSA University, Jalan SP2, Bandar Saujana Putra, Kuala Langat, 42610, Jenjarom, Selangor, Malaysia. .,School of Pharmacy, Faculty of Health & Medical Sciences, Taylor's University, No. 1 Jalan Taylor's, 47500, Subang Jaya, Selangor Darul Ehsan, Malaysia.
May Lee Low Department of Pharmaceutical Chemistry, School of Pharmacy, International Medical University, No. 126, Jalan Jalil Perkasa 19, 57000, Bukit Jalil, Kuala Lumpur, Malaysia
Ji Hui Lim Faculty of Pharmacy, MAHSA University, Jalan SP2, Bandar Saujana Putra, Kuala Langat, 42610, Jenjarom, Selangor, Malaysia
Yan Zhi Lor Faculty of Pharmacy, MAHSA University, Jalan SP2, Bandar Saujana Putra, Kuala Langat, 42610, Jenjarom, Selangor, Malaysia
Rusyidah Zainol Abidin Faculty of Pharmacy, MAHSA University, Jalan SP2, Bandar Saujana Putra, Kuala Langat, 42610, Jenjarom, Selangor, Malaysia
Vilasini Eh Dam Faculty of Pharmacy, MAHSA University, Jalan SP2, Bandar Saujana Putra, Kuala Langat, 42610, Jenjarom, Selangor, Malaysia
Napsiah Abdul Rahman Laboratory of Vaccines and Immunotherapeutics, Institute of Bioscience, Universiti Putra Malaysia (UPM), 43400, Serdang, Selangor, Malaysia
Chaw Yee Beh Laboratory of Vaccines and Immunotherapeutics, Institute of Bioscience, Universiti Putra Malaysia (UPM), 43400, Serdang, Selangor, Malaysia
Lee Chin Chan Virology Lab 1, Faculty of Biotechnology and Biomolecular Sciences, Universiti Putra Malaysia (UPM), 43400, Serdang, Selangor, Malaysia
Chee Wun How Faculty of Pharmacy, MAHSA University, Jalan SP2, Bandar Saujana Putra, Kuala Langat, 42610, Jenjarom, Selangor, Malaysia
Yin Sim Tor School of Biosciences, Faculty of Health & Medical Sciences, Taylor's University, No. 1 Jalan Taylor's, 47500, Subang Jaya, Selangor Darul Ehsan, Malaysia
Latifah Saiful Yazan Laboratory of Vaccines and Immunotherapeutics, Institute of Bioscience, Universiti Putra Malaysia (UPM), 43400, Serdang, Selangor, Malaysia.,Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia (UPM), 43400, Serdang, Selangor, Malaysia

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Bonde GV, Yadav SK, Chauhan S, Mittal P, Ajmal G, Thokala S, Mishra B. Lapatinib nano-delivery systems: a promising future for breast cancer treatment. Expert Opin Drug Deliv 2018. [DOI: 10.1080/17425247.2018.1449832] [Citation(s) in RCA: 16] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/19/2022]

Ong MS, Cai W, Yuan Y, Leong HC, Tan TZ, Mohammad A, You ML, Arfuso F, Goh BC, Warrier S, Sethi G, Tolwinski NS, Lobie PE, Yap CT, Hooi SC, Huang RY, Kumar AP. 'Lnc'-ing Wnt in female reproductive cancers: therapeutic potential of long non-coding RNAs in Wnt signalling. Br J Pharmacol 2017;174:4684-4700. [PMID: 28736855 PMCID: PMC5727316 DOI: 10.1111/bph.13958] [Citation(s) in RCA: 59] [Impact Index Per Article: 7.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/01/2017] [Revised: 06/30/2017] [Accepted: 07/17/2017] [Indexed: 02/06/2023] Open

Abstract

Recent discoveries in the non-coding genome have challenged the original central dogma of molecular biology, as non-coding RNAs and related processes have been found to be important in regulating gene expression. MicroRNAs and long non-coding RNAs (lncRNAs) are among those that have gained attention recently in human diseases, including cancer, with the involvement of many more non-coding RNAs (ncRNAs) waiting to be discovered. ncRNAs are a group of ribonucleic acids transcribed from regions of the human genome, which do not become translated into proteins, despite having essential roles in cellular physiology. Deregulation of ncRNA expression and function has been observed in cancer pathogenesis. Recently, the roles of a group of ncRNA known as lncRNA have gained attention in cancer, with increasing reports of their oncogenic involvement. Female reproductive cancers remain a leading cause of death in the female population, accounting for almost a third of all female cancer deaths in 2016. The Wnt signalling pathway is one of the most important oncogenic signalling pathways which is hyperactivated in cancers, including female reproductive cancers. The extension of ncRNA research into their mechanistic roles in human cancers has also led to novel reported roles of ncRNAs in the Wnt pathway and Wnt-mediated oncogenesis. This review aims to provide a critical summary of the respective roles and cellular functions of Wnt-associated lncRNAs in female reproductive cancers and explores the potential of circulating cell-free lncRNAs as diagnostic markers and lncRNAs as therapeutic targets.

LINKED ARTICLES

This article is part of a themed section on WNT Signalling: Mechanisms and Therapeutic Opportunities. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.24/issuetoc.

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Affiliation(s)

Mei S Ong Departments of Physiology, Yong Loo Lin School of MedicineNational University of SingaporeSingapore
Wanpei Cai Departments of Pharmacology, Yong Loo Lin School of MedicineNational University of SingaporeSingapore Cancer Science Institute of SingaporeNational University of SingaporeSingapore
Yi Yuan Cancer Science Institute of SingaporeNational University of SingaporeSingapore
Hin C Leong Departments of Pharmacology, Yong Loo Lin School of MedicineNational University of SingaporeSingapore Cancer Science Institute of SingaporeNational University of SingaporeSingapore
Tuan Z Tan Cancer Science Institute of SingaporeNational University of SingaporeSingapore
Asad Mohammad Cancer Science Institute of SingaporeNational University of SingaporeSingapore
Ming L You Cancer Science Institute of SingaporeNational University of SingaporeSingapore
Frank Arfuso Stem Cell and Cancer Biology Laboratory, School of Biomedical Sciences, Curtin Health Innovation Research InstituteCurtin UniversityPerthWAAustralia
Boon C Goh Departments of Pharmacology, Yong Loo Lin School of MedicineNational University of SingaporeSingapore Cancer Science Institute of SingaporeNational University of SingaporeSingapore National University Cancer InstituteNational University Health SystemSingapore Department of Haematology‐OncologyNational University Health SystemSingapore
Sudha Warrier Division of Cancer Stem Cells and Cardiovascular Regeneration, Manipal Institute of Regenerative MedicineManipal UniversityBangaloreIndia School of Biomedical Sciences, Curtin Health Innovation Research InstituteCurtin UniversityPerthWAAustralia
Gautam Sethi Departments of Pharmacology, Yong Loo Lin School of MedicineNational University of SingaporeSingapore School of Biomedical Sciences, Curtin Health Innovation Research InstituteCurtin UniversityPerthWAAustralia
Nicholas S Tolwinski Division of ScienceYale‐NUS CollegeSingapore Department of Biological ScienceNational University of SingaporeSingapore
Peter E Lobie Departments of Pharmacology, Yong Loo Lin School of MedicineNational University of SingaporeSingapore Departments of Anatomy, Yong Loo Lin School of MedicineNational University of SingaporeSingapore Tsinghua Berkeley Shenzhen Institute and Division of Life Science and HealthTsinghua University Graduate SchoolShenzhenChina
Celestial T Yap Departments of Physiology, Yong Loo Lin School of MedicineNational University of SingaporeSingapore National University Cancer InstituteNational University Health SystemSingapore
Shing C Hooi Departments of Physiology, Yong Loo Lin School of MedicineNational University of SingaporeSingapore
Ruby Y Huang Departments of Anatomy, Yong Loo Lin School of MedicineNational University of SingaporeSingapore Cancer Science Institute of SingaporeNational University of SingaporeSingapore National University Cancer InstituteNational University Health SystemSingapore Department of Obstetrics and GynaecologyNational University HospitalSingapore
Alan P Kumar Departments of Pharmacology, Yong Loo Lin School of MedicineNational University of SingaporeSingapore Cancer Science Institute of SingaporeNational University of SingaporeSingapore National University Cancer InstituteNational University Health SystemSingapore Division of Cancer Stem Cells and Cardiovascular Regeneration, Manipal Institute of Regenerative MedicineManipal UniversityBangaloreIndia Curtin Medical School, Faculty of Health ScienceCurtin UniversityPerthWAAustralia Department of Biological SciencesUniversity of North TexasDentonTXUSA

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Chan CWH, Law BMH, So WKW, Chow KM, Waye MMY. Novel Strategies on Personalized Medicine for Breast Cancer Treatment: An Update. Int J Mol Sci 2017;18:ijms18112423. [PMID: 29140300 PMCID: PMC5713391 DOI: 10.3390/ijms18112423] [Citation(s) in RCA: 50] [Impact Index Per Article: 6.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/27/2017] [Revised: 11/10/2017] [Accepted: 11/13/2017] [Indexed: 12/22/2022] Open

Sorace AG, Harvey S, Syed A, Yankeelov TE. Imaging Considerations and Interprofessional Opportunities in the Care of Breast Cancer Patients in the Neoadjuvant Setting. Semin Oncol Nurs 2017;33:425-439. [PMID: 28927763 DOI: 10.1016/j.soncn.2017.08.008] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/17/2022]

Padayachee ER, Biteghe FAN, Malindi Z, Bauerschlag D, Barth S. Human Antibody Fusion Proteins/Antibody Drug Conjugates in Breast and Ovarian Cancer. Transfus Med Hemother 2017;44:303-310. [PMID: 29070975 DOI: 10.1159/000479979] [Citation(s) in RCA: 8] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/03/2017] [Accepted: 08/01/2017] [Indexed: 12/19/2022] Open

Abstract

Considerable research efforts have been dedicated to understanding ovarian and breast cancer mechanisms, but there has been little progress translating the research into effective clinical applications. Hence, personalized/precision medicine has emerged because of its potential to improve the accuracy of tumor targeting and minimize toxicity to normal tissue. Targeted therapy in both breast and ovarian cancer has focused on antibodies, antibody drug conjugates (ADCs), and very recently the introduction of human antibody fusion proteins. Small molecule inhibitors and monoclonal antibodies (mAbs) are used in conjunction with chemotherapeutic drugs as a form of treatment but problems arise from a board expression of the target antigen in healthy tissues. Also, insufficient tumor penetration due to tight binding affinity and macromolecular size of mAbs compromise the efficacy of these ADCs. A more targeted approach is thus needed, and ADCs were designed to meet this need. However, in ADCs the method of conjugation of drug to antibody is >1, altering the structure of the drug which leads to off-target effects. Random conjugation also causes the drug to affect the pharmokinetics and biodistribution of the antibody and may cause nonspecific binding and internalization. Recombinant therapeutic proteins achieve controlled conjugation reactions and combine cytotoxicity and targeting in one molecule. They can also be engineered to extend half-life, stability and mechanism of action, and offer novel delivery routes. SNAP-tag fusion proteins are an example of a theranostic recombinant protein as they provide a unique antibody format to conjugate a variety of benzyl guanine modified labels, e.g. fluorophores and photosensitizers in a 1:1 stoichiometry. On the one hand, SNAP tag fusions can be used to optically image tumors when conjugated to a fluorophore, and on the other hand the recombinant proteins can induce necrosis/apoptosis in the tumor when conjugated to a photosensitizer upon exposure to a changeable wavelength of light. The dual nature of SNAP-tag fusions as both a diagnostic and therapeutic tool reinforces its significant role in cancer treatment in an era of precision medicine.

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Arora R, Krishnan V. Selective Targeting of the L858R Mutation (EGFR) in Non-Small Cell Lung Cancer: A Mechanism for Advancing Targeted Chemotherapy. Front Oncol 2017;7:104. [PMID: 28611939 PMCID: PMC5447734 DOI: 10.3389/fonc.2017.00104] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/19/2016] [Accepted: 05/05/2017] [Indexed: 01/06/2023] Open

Masoud V, Pagès G. Targeted therapies in breast cancer: New challenges to fight against resistance. World J Clin Oncol 2017;8:120-134. [PMID: 28439493 PMCID: PMC5385433 DOI: 10.5306/wjco.v8.i2.120] [Citation(s) in RCA: 215] [Impact Index Per Article: 26.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/19/2016] [Revised: 09/16/2016] [Accepted: 10/17/2016] [Indexed: 02/06/2023] Open

Xie Y, Qi Y, Zhang Y, Chen J, Wu T, Gu Y. Regulation of angiogenic factors by the PI3K/Akt pathway in A549 lung cancer cells under hypoxic conditions. Oncol Lett 2017;13:2909-2914. [PMID: 28521397 PMCID: PMC5431373 DOI: 10.3892/ol.2017.5811] [Citation(s) in RCA: 8] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/05/2016] [Accepted: 11/02/2016] [Indexed: 01/24/2023] Open

Abstract

The aim of the present study was to investigate the influence of hypoxia and PI3K inhibition on angiogenic factors in A549 lung cancer cells. A549 cells were treated with the PI3K inhibitor LY294002 under normoxic and hypoxic conditions. Untreated cells were used as the control group and those treated by the inhibitor, as the suppression group. The cells were further divided based on normoxic or hypoxic conditions and named: Normoxic control group, normoxic suppression group, hypoxic control group and hypoxic suppression group. Expression levels of hypoxia-inducible factor (HIF)-1α and AKT1 mRNA in all groups were determined by reverse transcriptase-quantitative polymerase chain reaction and concentrations of vascular endothelial growth factor (VEGF), angiotensin II (ANG-II), transforming growth factor (TGF)-α/β1, and tumor necrosis factor (TNF)-α in the culture supernatant were measured by enzyme-linked immunosorbent assay. The expression levels of HIF-1α and AKT1 mRNA in the hypoxic control group were higher than those in the normoxic control group and the expression levels of HIF-1α and AKT1 mRNA in the hypoxic control group were higher than those in the hypoxic suppression group. Compared to the normoxic control and normoxic suppression groups, the concentrations of VEGF and TNF-α in supernatant were higher in the hypoxic control and hypoxic suppression groups, respectively. However, TGF-α and TGF-β1 demonstrated the opposite trend of the aforementioned factors. The concentration of ANG-II in the hypoxic suppression group was higher than that in the normoxic suppression group. In addition, compared to the normoxic control group and hypoxic control group, the concentrations of VEGF and TGF-β1 in supernatant were lower in the normoxic suppression group and in the hypoxic suppression group, respectively. In conclusion, the results of the present study suggest that hypoxia can stimulate A549 lung cancer cells to secrete VEGF and TNF-α and inhibit TGF-α and TGF-β1. The ability of A549 cells to secrete VEGF and TGF-β1 is regulated by PI3K/Akt, and ANG-II expression may be regulated by the PI3K/Akt pathway under hypoxic condition.

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Gastelum GM, Iqbal C, Hilsenbeck SG, Rimawi MF, Niravath P. Retrospective review of genomic testing in breast cancer: Does it improve outcome? Breast Cancer Res Treat 2017;163:191-195. [PMID: 28224382 DOI: 10.1007/s10549-017-4154-3] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/07/2017] [Accepted: 02/09/2017] [Indexed: 10/20/2022]

Vanderpuye V, Grover S, Hammad N, PoojaPrabhakar, Simonds H, Olopade F, Stefan DC. An update on the management of breast cancer in Africa. Infect Agent Cancer 2017;12:13. [PMID: 28228841 PMCID: PMC5307840 DOI: 10.1186/s13027-017-0124-y] [Citation(s) in RCA: 105] [Impact Index Per Article: 13.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/17/2016] [Accepted: 02/03/2017] [Indexed: 01/04/2023] Open

Abstract

Background

There is limited information about the challenges of cancer management and attempts at improving outcomes in Africa. Even though South and North Africa are better resourceds to tackle the burden of breast cancer, similar poor prognostic factors are common to all countries. The five-year overall Survival rate for breast cancer patients does not exceed 60% for any low and middle-income country (LMIC) in Africa. In spite of the gains achieved over the past decade, certain characteristics remain the same such as limited availability of breast conservation therapies, inadequate access to drugs, few oncology specialists and adherence to harmful socio-cultural practices. This review on managing breast cancer in Africa is authored by African oncologists who practice or collaborate in Africa and with hands-on experience with the realities.

Methods

A search was performed via electronic databases from 1999 to 2016. (PubMed/Medline, African Journals Online) for all literature in English or translated into English, covering the terms “breast cancer in Africa and developing countries”. One hundred ninety were deemed appropriate.

Results

Breast tumors are diagnosed at earlier ages and later stages than in highincome countries. There is a higher prevalence of triple-negative cancers. The limitations of poor nursing care and surgery, inadequate access to radiotherapy, poor availability of basic and modern systemic therapies translate into lower survival rate. Positive strides in breast cancer management in Africa include increased adaptation of treatment guidelines, improved pathology services including immuno-histochemistry, expansion and upgrading of radiotherapy equipment across the continent in addition to more research opportunities.

Conclusion

This review is an update of the management of breast cancer in Africa, taking a look at the epidemiology, pathology, management resources, outcomes, research and limitations in Africa from the perspective of oncologists with local experience.

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Takeda T, Yamamoto H, Kanzaki H, Suzawa K, Yoshioka T, Tomida S, Cui X, Murali R, Namba K, Sato H, Torigoe H, Watanabe M, Shien K, Soh J, Asano H, Tsukuda K, Kitamura Y, Miyoshi S, Sendo T, Toyooka S. Yes1 signaling mediates the resistance to Trastuzumab/Lap atinib in breast cancer. PLoS One 2017;12:e0171356. [PMID: 28158234 PMCID: PMC5291431 DOI: 10.1371/journal.pone.0171356] [Citation(s) in RCA: 32] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/29/2016] [Accepted: 01/19/2017] [Indexed: 12/13/2022] Open

Abstract

Background

Overexpression of human epidermal growth factor receptor 2 (HER2) is observed in approximately 15–23% of breast cancers and these cancers are classified as HER2-positive breast cancer. Trastuzumab is the first-line targeted therapeutic drug for HER2-positive breast cancer and has improved patient overall survival. However, acquired resistance to trastuzumab is still a critical issue in breast cancer treatment. We previously established a trastuzumab-resistant breast cancer cell line (named as BT-474-R) from a trastuzumab-sensitive HER2-amplified cell line BT-474. Lapatinib is also a molecular-targeted drug for HER2-positive breast cancer, which acquired the resistance to trastuzumab. Acquired resistance to lapatinib is also an issue to be conquered.

Methods

We established trastuzumab/lapatinib-dual resistant cell line (named as BT-474-RL2) by additionally treating BT-474-R with lapatinib. We analyzed the mechanisms of resistance to trastuzumab and lapatinib. Besides, we analyzed the effect of the detected resistance mechanism in HER2-positive breast cancer patients.

Results

Proto-oncogene tyrosine-protein kinase Yes1, which is one of the Src family members, was amplified, overexpressed and activated in BT-474-R and BT-474-RL2. Silencing of Yes1 by siRNA induced both BT-474-R and BT-474-RL2 to restore the sensitivity to trastuzumab and lapatinib. Pharmaceutical inhibition of Yes1 by the Src inhibitor dasatinib was also effective to restore the sensitivity to trastuzumab and lapatinib in the two resistant cell lines. Combination treatment with dasatinib and trastuzumab induced down-regulation of signaling molecules such as HER2 and Akt. Moreover, the combination treatments induced G1-phase cell-cycle arrest and apoptosis. Consistent with cell line data, high expression of Yes1 mRNA was correlated with worse prognosis in patients with HER2-positive breast cancer.

Conclusion

Yes1 plays an important role in acquired resistance to trastuzumab and lapatinib in HER2-positive breast cancer. Our data suggest that pharmacological inhibition of Yes1 may be an effective strategy to overcome resistance to trastuzumab and lapatinib.

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Affiliation(s)

Tatsuaki Takeda Department of Clinical Pharmacy, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan
Hiromasa Yamamoto Department of Thoracic, Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan
Hirotaka Kanzaki Department of Clinical Pharmacy, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan
Ken Suzawa Department of Thoracic, Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan
Takahiro Yoshioka Department of Clinical Genomic Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan
Shuta Tomida Department of Biobank, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan
Xiaojiang Cui Department of Surgery, Cedars-Sinai Medical Center, Los Angeles, California, United States of America
Ramachandran Murali Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, California, United States of America
Kei Namba Department of Thoracic, Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan
Hiroki Sato Department of Thoracic, Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan
Hidejiro Torigoe Department of Thoracic, Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan Department of Clinical Genomic Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan
Mototsugu Watanabe Department of Thoracic, Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan
Kazuhiko Shien Department of Thoracic, Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan
Junichi Soh Department of Thoracic, Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan
Hiroaki Asano Department of Thoracic, Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan
Kazunori Tsukuda Department of Thoracic, Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan
Yoshihisa Kitamura Department of Clinical Pharmacy, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan
Shinichiro Miyoshi Department of Thoracic, Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan
Toshiaki Sendo Department of Clinical Pharmacy, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan
Shinichi Toyooka Department of Thoracic, Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan Department of Clinical Genomic Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan * E-mail:

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Sebastian A, Pandey V, Mohan CD, Chia YT, Rangappa S, Mathai J, Baburajeev CP, Paricharak S, Mervin LH, Bulusu KC, Fuchs JE, Bender A, Yamada S, Lobie PE, Rangappa KS. Novel Adamantanyl-Based Thiadiazolyl Pyrazoles Targeting EGFR in Triple-Negative Breast Cancer. ACS OMEGA 2016;1:1412-1424. [PMID: 30023509 PMCID: PMC6044684 DOI: 10.1021/acsomega.6b00251] [Citation(s) in RCA: 32] [Impact Index Per Article: 3.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Figures] [Subscribe] [Scholar Register] [Received: 09/18/2016] [Accepted: 12/15/2016] [Indexed: 06/08/2023]

Affiliation(s)

Anusha Sebastian Laboratory of Chemical Biology, Department of Chemistry, Bangalore University, Central College campus, Palace Road, Bangalore560001, India
Vijay Pandey Cancer Science Institute of Singapore and Department of Pharmacology, National University of Singapore, 14 Medical Drive #11-02, MD6, Singapore 117599, Singapore
Chakrabhavi Dhananjaya Mohan Department of Studies in Chemistry and Department of Studies in Molecular Biology, University of Mysore, Manasagangotri, Mysore 570006, India
Yi Ting Chia Cancer Science Institute of Singapore and Department of Pharmacology, National University of Singapore, 14 Medical Drive #11-02, MD6, Singapore 117599, Singapore
Shobith Rangappa Frontier Research Center for Post-Genome Science and Technology, Hokkaido University, Sapporo 060-0808, Japan
Jessin Mathai Centre for Advanced Biomedical Research and Innovation, Gulf Medical University, Ajman 4184, United Arab Emirates
C. P. Baburajeev Laboratory of Chemical Biology, Department of Chemistry, Bangalore University, Central College campus, Palace Road, Bangalore560001, India
Shardul Paricharak Department of Chemistry, Centre for Molecular Informatics, University of Cambridge, Lensfield Road, Cambridge CB2 1EW, U.K. Division of Medicinal Chemistry, Leiden Academic Centre for Drug Research, Leiden University, P.O. Box 9502, Leiden 2300 RA, The Netherlands
Lewis H. Mervin Department of Chemistry, Centre for Molecular Informatics, University of Cambridge, Lensfield Road, Cambridge CB2 1EW, U.K.
Krishna C. Bulusu Department of Chemistry, Centre for Molecular Informatics, University of Cambridge, Lensfield Road, Cambridge CB2 1EW, U.K.
Julian E. Fuchs Department of Chemistry, Centre for Molecular Informatics, University of Cambridge, Lensfield Road, Cambridge CB2 1EW, U.K.
Andreas Bender Department of Chemistry, Centre for Molecular Informatics, University of Cambridge, Lensfield Road, Cambridge CB2 1EW, U.K.
Shuhei Yamada Department of Pathobiochemistry, Faculty of Pharmacy, Meijo University, Nagoyo 468-8503, Japan
Peter E. Lobie Cancer Science Institute of Singapore and Department of Pharmacology, National University of Singapore, 14 Medical Drive #11-02, MD6, Singapore 117599, Singapore
Kanchugarakoppal S. Rangappa Department of Studies in Chemistry and Department of Studies in Molecular Biology, University of Mysore, Manasagangotri, Mysore 570006, India

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Lv Q, Meng Z, Yu Y, Jiang F, Guan D, Liang C, Zhou J, Lu A, Zhang G. Molecular Mechanisms and Translational Therapies for Human Epidermal Receptor 2 Positive Breast Cancer. Int J Mol Sci 2016;17:E2095. [PMID: 27983617 PMCID: PMC5187895 DOI: 10.3390/ijms17122095] [Citation(s) in RCA: 41] [Impact Index Per Article: 4.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/05/2016] [Revised: 11/15/2016] [Accepted: 12/01/2016] [Indexed: 12/16/2022] Open

Affiliation(s)

Quanxia Lv Institute for Advancing Translational Medicine in Bone & Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University (HKBU), Hong Kong 999077, China. Institute of Precision Medicine and Innovative Drug Discovery, HKBU (Haimen) Institute of Science and Technology (IST), Haimen 226133, China.
Ziyuan Meng Institute for Advancing Translational Medicine in Bone & Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University (HKBU), Hong Kong 999077, China. Institute of Precision Medicine and Innovative Drug Discovery, HKBU (Haimen) Institute of Science and Technology (IST), Haimen 226133, China.
Yuanyuan Yu Institute for Advancing Translational Medicine in Bone & Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University (HKBU), Hong Kong 999077, China.
Feng Jiang Institute for Advancing Translational Medicine in Bone & Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University (HKBU), Hong Kong 999077, China. Institute of Precision Medicine and Innovative Drug Discovery, HKBU (Haimen) Institute of Science and Technology (IST), Haimen 226133, China. The State Key Laboratory Base of Novel Functional Materials and Preparation Science, Faculty of Materials Science and Chemical Engineering, Ningbo University, Ningbo 315211, China.
Daogang Guan Institute for Advancing Translational Medicine in Bone & Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University (HKBU), Hong Kong 999077, China.
Chao Liang Institute for Advancing Translational Medicine in Bone & Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University (HKBU), Hong Kong 999077, China.
Junwei Zhou Institute for Advancing Translational Medicine in Bone & Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University (HKBU), Hong Kong 999077, China.
Aiping Lu Institute for Advancing Translational Medicine in Bone & Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University (HKBU), Hong Kong 999077, China. Institute of Precision Medicine and Innovative Drug Discovery, HKBU (Haimen) Institute of Science and Technology (IST), Haimen 226133, China.
Ge Zhang Institute for Advancing Translational Medicine in Bone & Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University (HKBU), Hong Kong 999077, China. Institute of Precision Medicine and Innovative Drug Discovery, HKBU (Haimen) Institute of Science and Technology (IST), Haimen 226133, China.

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Abstract

In the current study, the prognostic and predictive values of serum transforming growth factor-β1 (TGF-β1), insulin-like growth factor I (IGF-I)/IGF-I receptor (IGF-IR) and vascular endothelial growth factor-A (VEGF-A) were evaluated in triple-negative and non-triple-negative breast cancer (TNBC and non-TNBC). The aim was to identify a group of serological biomarkers and to identify possible candidates for targeted therapy in patients with TNBC and non-TNBC. Protein levels of TGF-β1, IGF-I/IGF-IR and VEGF-A in the serum were measured in 43 TNBC, 53 non-TNBC and 20 normal control participants using quantitative ELISA assays. Results were correlated against standard prognostic factors, response to treatment and survival. TNBC was identified to be associated with poor prognosis and serum levels of VEGF-A and IGF/IGF-IR were significantly higher in the TNBC group compared with the non-TNBC group. IGF-IR and VEGF-A overexpression was observed to be correlated with TGF-β1 expression and all of the markers investigated were associated with metastasis and disease progression. In the multivariate analysis, VEGF-A, IGF-I and IGF-IR were observed to be independent predictors for overall survival, whereas TGF-β1 and lymph node status were identified as independent predictors for disease-free survival. The overall response rate was significantly lower in patients with TNBC and those with high levels of TGF-β1, IGF-I/IGF-IR and VEGF-A. In view of the present results, it was concluded that TGF-β1, IGF-I/IGF-IR and VEGF-A overexpression is associated with the presence of aggressive tumors, which exhibit an increased probability of metastasis, a poor response to treatment and reduced survival rate. This indicates that VEGF-A, IGF-IR and IGF-I have the potential to be used as surrogate biomarkers and are promising candidates for targeted therapy, particularly in patients with TNBC.

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